Publications by authors named "Bedigian H"

To assess the impact of room ventilation on animal cage microenvironment, intracage ventilation rate, temperature, humidity, and concentrations of carbon dioxide and ammonia were monitored in nonpressurized, bonnet-topped mouse cages. Cages on the top, middle, and bottom rows of a mouse rack were monitored at room ventilation rates of 0, 5, 10, and 20 air changes/h (ACH). Ventilation inside the animal cage increased somewhat from 12.

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The LIP-6 MAb was produced against the undifferentiated cell line bh2-1 and recognizes an antigen expressed on all pre-B and B cell lines tested and some myeloid lineage lines. FACS analysis of normal tissues showed that LIP-6 is expressed on B lineage cells at all stages of differentiation, from bone marrow pre-B to plasma cells. T cells and thymocytes are LIP-6-, and splenic CD11b+ cells are heterogeneous for LIP-6 expression.

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Evi-2, a common site of viral integration in BXH-2 myeloid lymphomas, is located within a large intron of the Nf1 tumor suppressor gene. Viral integration at Evi-2 appears to induce disease by disrupting normal Nf1 expression. During our attempts to characterize the nature of the proviruses located at Evi-2, we found that approximately half of the proviruses were defective nonecotropic proviruses (A.

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Background/aims: C3H/HeJ mice at the Jackson Laboratory have periodically been culled because of the occurrence of soft feces, perianal ulceration, and right-sided colitis. No pathogens have been isolated. The goal of the current study was to establish a substrain with a high incidence of this disease.

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Recombinant inbred BXH-2 mice spontaneously produce a B-tropic murine leukemia virus (MuLV) beginning early in life and have a high incidence of spontaneous myeloid leukemia. These traits are not characteristic of the progenitor strains (C57BL/6J and C3H/HeJ) or of 11 other recombinant inbred BXH strains. Genetic analysis has shown that the virus is not transmitted through the germ line, suggesting that the virus is passed from one generation to the next by horizontal transmission.

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Polymerase chain reaction (PCR) based on single primers of arbitrary nucleotide sequence provides a powerful marker system for genome analysis because each primer amplifies multiple products, and cloning, sequencing, and hybridization are not required. We have evaluated this typing system for the mouse by identifying optimal PCR conditions; characterizing effects of GC content, primer length, and multiplexed primers; demonstrating considerable variation among a panel of inbred strains; and establishing linkage for several products. Mg2+, primer, template, and annealing conditions were identified that optimized the number and resolution of amplified products.

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Myoepitheliomas are subcutaneous tumors that arise from myoepithelial cells of various exocrine glands. In a retrospective study of 142 tumors observed over a period of 3 years, myoepitheliomas occurred spontaneously in A/HeJ, A/J, BALB/cJ, BALB/cByJ, LLC.A/Ckc, and NOD/Lt inbred strains of mice.

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A total of 14 well differentiated rhabdomyosarcomas were diagnosed at necropsy in 10,000 mice. Of the 14 affected mice, ten were BALB/cJ, and there was one case each of A/HeJ, BALB/cByJ, C58/J, and C.B-17-scid/scid strains.

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BXH-2 mice have the highest incidence of spontaneous retrovirally induced myeloid leukemia of any known inbred strain and, as such, represent a valuable model system for identifying cellular proto-oncogenes involved in myeloid disease. Chronic murine leukemia viruses often induce disease by insertional activation or mutation of cellular proto-oncogenes. These loci are identified as common viral integration sites in tumor DNAs.

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An epithelial cell line (RC-4B/C) was established from a pituitary adenoma obtained from a 3-yr-old (ACI/fMai X F344/fMai)F1 male rat. Before Year 5 in vitro, RC-4B/C cells could not be viably recovered from cryogenic storage. Recovery of viable cells from cryogenic storage in Year 5 was associated with a more transformed phenotype, including the appearance of endogenous C-type rat retroviral particles.

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Various procedures were utilized to determine the most sensitive, cost and labor effective techniques for detection of Pneumocystis carinii in immunologically compromised mice. Immunoperoxidase staining techniques that utilized polyclonal antibodies directed against purified rat or mouse P. carinii were more sensitive and specific than staining with Gomori's methenamine silver.

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The inbred mouse strain CWD/LeAgl, which has a high incidence of spontaneous B-cell lymphomas, expresses both ecotropic MuLV and MCF viruses. Studies indicated that the MCF viruses expressed in CWD tumors were characteristic of nononcogenic MCF viruses and that ecotropic MuLV may be the etiological agent in spontaneous B-cell lymphomagenesis. Somatically acquired proviruses of approximately the same size were detected in several tumor DNAs suggesting that integration of proviral sequences into specific regions of the mouse genome may be an important step in lymphomagenesis of this strain.

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Previous studies of 21 highly lymphomatous AKXD recombinant inbred mouse strains demonstrated correlations between lymphoma type, the somatic proviral DNA content of the lymphoma, and the frequency of virally induced rearrangements in eight common sites of viral integration (Myc, Pim-i, Pvt-1, Mlvi-1, Mlvi-2, Fis-1, Myb, and Evi-1). In this study we analyzed lymphomas from six inbred mouse strains, AKR/J, C58/J, HRS/J (hr/hr and hr/+), SJL/J, SEA/GnJ, and CWD/LeAgl, to determine whether these correlations are also evident in these strains. Mice of the AKR/J, C58/J, and HRS/J strains died exclusively of T-cell lymphomas.

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A common site of ecotropic murine leukemia virus integration designated Evi-2 (ecotropic viral integration site-2) has been identified in BXH-2 myeloid tumors. As part of experiments to determine whether Evi-2 identified a new proto-oncogene locus involved in myeloid disease, we determined its chromosomal location. We mapped Evi-2 to mouse Chromosome 11 using standard recombinant inbred strain and genetic backcross analysis.

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Lymph node cells from C3H mice homozygous for lpr and gld were compared for expression of cell surface antigens, lectin-binding sites, functional characteristics, expression of ecotropic MuLV, and organization of Ig and T cell receptor (TcR) beta-chain genes. The abnormal cells (Ly-2-/L3T4-) populating nodes of both mutant strains were specifically purified by using plate separation techniques. The purified abnormal cells were shown to express the beta-chain of the TcR, to exhibit rearrangements of the beta-chain genes, and to express TcR beta and alpha gene mRNA, demonstrating the T cell origin of these populations.

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The inbred mouse strain CWD/Agl has a high incidence of spontaneous B-cell lymphomas characterized by gross splenomegaly and lymph node enlargement. The endogenous ecotropic retrovirus of CWD/Agl mice is expressed in the spleen within the first 2 weeks of age and in the thymus by 1 month of age. Endogenous xenotropic virus is expressed in the spleen and bone marrow of the earliest age group examined (4 months).

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BXH-2 recombinant inbred (RI) mice produce high titers of B-ecotropic murine leukemia virus beginning early in life and have a high incidence of non-T-cell leukemias that occur before 1 year of age. The leukemias that develop are in some cases associated with hind limb paralysis. In addition, a dualtropic mink cell focus-forming virus has been isolated from leukemic cells of BXH-2 mice.

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Endogenous ecotropic murine leukemia virus expression varies with inbred mouse strain and age. The mechanism(s) regulating virus expression is unknown, but expression is thought to be controlled at the transcriptional level by linkage to cis-acting cellular DNA sequences or DNA methylation or both. To begin to differentiate between these different control mechanisms, we molecularly cloned two endogenous ecotropic proviruses, Emv-3 and Emv-13, complete with flanking cellular DNA sequences.

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All AKR/J mice carry at least three endogenous ecotropic viral loci which have been designated Emv-11 (Akv-1), Emv-13 (Akv-3), and Emv-14 (Akv-4) (Jenkins et al., J. Virol.

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